if you would like to check it out – the  website to do so is at the end of the article.
Hi Everyone

I am passing this email forwarded to me this morning. It’s about a

medication that is familiar to many of us. Note also the FDA ‘s comments

at the end of the message.

I received this information from a friend whose mother recently passed away.

Apparently, this was caused by a medication that is deadly. Here are the details and I suggest you pass it on to your loved ones and others.

Phenylpropanolamine (PPA)

I would like to thank those of you who expressed condolences on the recent passing of my mother.  She suffered a hemorrhagic stroke while she was driving home from my house at 7:30 and passed away at 8:30.   My mother’s stroke and passing was an enormous shock to my family because she did not have any symptoms or risk factors for a stroke. Just the week before she had gone to her doctor for a check up and received a clean bill of health.  She did, however, develop a cold while she was visiting me and had taken Alka Seltzer Cold Plus for 3 days.  Since her passing, we have learned that Alka Seltzer is one of the many cold medicines that contains Phenylpropanolamine (PPA) which can cause hemorrhagic strokes  (cerebral bleeding) even with the first use.  I am forwarding a list of other medications that currently use PPA. These medicines are supposedly being recalled but my mother just purchased this medication less than two weeks ago.  Pharmaceutical companies

have known about this danger for years, we unfortunately, did not.

I urge you to review the list of medicines with PPA and avoid these medications.   All drugs containing PHENYLPROPANOLAMINE are dangerous.  You may want to try calling the 800 number listed on most drug boxes and inquire about a REFUND.   Please read this CAREFULLY.   Also, please pass this on to everyone you know.  STOP TAKING anything containing this ingredient.  It has been linked to increased hemorrhagic stroke (bleeding in brain) among women ages 18-49 in the three days after starting use of medication.  Problems were not found in men, but the FDA recommended that everyone (even children) seek alternative medicine.

The following medications contain Phenylpropanolamine:

Acutrim Diet Gum Appetite Suppressant

Acutrim Plus Dietary Supplements

Acutrim Maximum Strength Appetite Control

Alka-Seltzer Plus Children’s Cold Medicine Effervescent

Alka-Seltzer Plus Cold medicine (cherry or or ange)

Alka-Seltzer Plus Cold Medicine Original

Alka-Seltzer Plus Cold & Cough Medicine Effervescent

Alka-Seltzer Plus Cold & Flu Medicine

Alka-Seltzer Plus Cold & Sinus Effervescent

Alka Seltzer Plus Night-Time Cold Medicine

BC Allergy Sinus Cold Powder

BC Sinus Cold Powder

Comtrex Flu Therapy & Fever Relief

Day & Night Contac 12-Hour Cold Capsules

Contac 12 Hour Caplets

Coricidin D Cold, Flu & Sinus

Dexatrim Caffeine Free

Dexatrim Extended Duration

Dexatrim Gelcaps

Dexatrim Vitamin C/Caffeine Free

Dimetapp Cold & Allergy Chewable Tablets

Dimetapp Cold & Cough Liqui-Gels

Dimetapp DM Cold & Cough Elixir

Dimetapp Elixir

Dimetapp 4 Hour Liquid Gels

Dimetapp 4 Hour Tablets

Dimetapp 12 Hour Extentabs Tablets

Naldecon DX Pediatric Drops

Permathene Mega-16

Robitussin CF

Tavist-D 12 Hour Relief of Sinus & Nasal Congestion

Triaminic DM Cough Rel! ief

Triaminic Expectorant Chest & Head

Triaminic Syrup ! ! Cold & amp; Allergy

Triaminic Triaminicol Cold & CoughI just found out and called the 800# on the container for Triaminic and

they informed me that they are voluntarily recalling the following medicines

because of a certain ingredient that is causing strokes and seizures in children:

Orange 3D Cold & Allergy Cherry (Pink)

3D Cold & Cough Berry

3D Cough Relief Yellow 3D Expectorant

They are asking you to call them at 800-548-3708 ; 800-548-3708 with the lot number on the box so they can send you postage for you to send it back to them, and they will also issue you a refund.   If you know of anyone else with small children,
PLEASE PASS THIS ON. THIS IS SERIOUS STUFF!
DO PASS ALONG TO ALL ON YOUR MAILING LIST so people are informed. They can then pass it along to their families.
To confirm these findings please take time to check the following:
http://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm150774.htm

  View News Source

View news sourece

Farshad Fani Marvasti, M.D., M.P.H., and Randall S. Stafford, M.D., Ph.D.

N Engl J Med 2012; 367:889-891September 6, 2012

Article

References

Although the United States pays more for medical care than any other country, problems abound in our health care system. Unsustainable costs, poor outcomes, frequent medical errors, poor patient satisfaction, and worsening health disparities all point to a need for transformative change.1Simultaneously, we face widening epidemics of obesity and chronic disease. Cardiovascular disease, cancer, and diabetes now cause 70% of U.S. deaths and account for nearly 75% of health care expenditures.2 Unfortunately, many modifiable risk factors for chronic diseases are not being addressed adequately. A prevention model, focused on forestalling the development of disease before symptoms or life-threatening events occur, is the best solution to the current crisis.

Disease prevention encompasses all efforts to anticipate the genesis of disease and forestall its progression to clinical manifestations. A focus on prevention does not imply that disease can be eliminated but instead embraces Fries’s model of “morbidity compression,”3 in which the disease-free life span is extended through the prevention of disease complications and the symptom burden is compressed into a limited period preceding death. Thus, a prevention model is ideally suited to addressing chronic conditions that take decades to develop and then manifest as life-threatening and ultimately fatal exacerbations.

Although the need for a prevention model was highlighted during the recent health care reform debate, efforts to expand prevention continue to be thwarted by a system better suited to acute care. A century after the Flexner report, the acute care model and its cultural, technological, and economic underpinnings remain securely embedded in every aspect of our health care system.

The organizational structure and function of our medical system is rooted in fundamental changes made at the beginning of the 20th century that emphasized an acute care approach and marginalized prevention and public health. Breakthroughs in laboratory sciences led by Koch and Pasteur provided powerful tools for mechanistically understanding and treating infectious diseases. Bolstered by philanthropy and the Flexner report, U.S. medicine became reliant on laboratory research.4 This strategy made sense 100 years ago, given the prominence of acute infectious diseases in a young population; it makes little sense now.

With the aging of the population, the shift in the burden of disease toward chronic conditions has accelerated. The most prevalent preventable causes of death are now obesity and smoking, which result in delayed but progressive disease.5 Even in the developing world, increases in the prevalence of chronic disease are outstripping reductions in acute infectious diseases.1 Such epidemiologic evolution demands a focus on public health and prevention.

Yet economic and technological factors dating from the early 20th century remain strong barriers to effective disease prevention. A key feature of U.S. health care is its use of a piecemeal, task-based system that reimburses for “sick visits” aimed at addressing acute conditions or acute exacerbations of chronic conditions. Economic incentives encourage overuse of services by favoring procedural over cognitive tasks (e.g., surgery versus behavior-change counseling) and specialty over primary care. The current model largely ignores subclinical disease unless risk factors are “medicalized” and asymptomatic persons are redefined as “diseased” to facilitate drug treatment. These mismatched economic incentives effectively preclude successful prevention through health maintenance.

Moreover, our reliance on ever newer, more advanced technology has perpetuated an expensive system in which costly new technology is widely adopted in the absence of comparative advantage. When combined with economic incentives for patenting devices and drugs, these technological factors become self-reinforcing. Although many preventive strategies may be cost-effective, they unfortunately have limited potential for wide adoption because they cannot be patented or made profitable. Therefore, the primacy of patentable therapies impedes research on prevention and diffusion of prevention approaches that could cost-effectively address the burden of chronic disease.

The cultural and social underpinnings of our system also inhibit optimal disease prevention. Faith in reductionism, which was infused into medicine in the 20th century, has empowered medical research to pursue only isolated problems and to yield targeted, immediately deployable solutions. Consequently, the model for treating acute infectious disease is being misapplied to the treatment of chronic disease. For example, cancer chemotherapy is modeled after antibiotic therapy, and coronary revascularization is modeled after abscess incision and débridement. Societal expectations of a “magic bullet” and a focus on symptom relief also reflect and reinforce the reductionist approach. These scientific and societal values emphasize discovering a “cure” for the major causes of death. With the advent of direct-to-consumer advertising for pharmaceuticals and surgical procedures, these cultural expectations of immediate, simplistic solutions have been bolstered by consumerism and fully exploited to generate demand for therapies that are marginally indicated and potentially unsafe. Our very culture thus devalues disease prevention.

Changing the system requires recognition of these cultural, technological, and economic obstacles and identification of specific means for overcoming them through alterations in medical education, medical research, health policy, and reimbursement. For example, to combat the primacy of technical knowledge and the profit-based system for medical technology, medical schools must teach prevention strategies alongside treatment approaches and emphasize motivational interviewing with a focus on lifestyle modification. Payers and the federal government must fully reward use of appropriate nonpatentable therapies and support research on the development and dissemination of prevention strategies.

To change our reductionist way of thinking, we must teach aspiring physicians about systems science that addresses psychological, social, and economic determinants of disease. Taking a patient-centered, whole-person approach focused on long-term functional status will also help to address the current fragmentation of care and allow for standardization of prevention strategies.

Medical school curricula should emphasize homeostasis and health, rather than only disease and diagnosis, and provide training in the science and practice of cost-effective health promotion. In turn, payers will need to reimburse for health maintenance and prevention activities, primary care physicians will have to act as health coaches, and all health care professionals will need to embrace a coordinated multidisciplinary team approach. Systematic steps must also be taken to change the culture of medicine so that primary care is valued. Renewing primary care will require increasing ambulatory care training in community settings and reallocating funding for residency training away from hospitals to reimburse appropriately for innovative models such as medical homes. Furthermore, we must compensate primary care physicians for their work as care coordinators by establishing reimbursement parity for cognitive and procedural care and accounting for long-term costs and benefits.

The new approach to medicine endorsed by the Flexner report succeeded because it was based on sound science and a radical restructuring of the way medicine was taught, organized, and practiced. Today, we face a similar challenge that requires another fundamental reordering of our health care system. Although the need for acute care will remain, centering our efforts on prevention is the only way to thwart the emerging pandemic of chronic disease.

Current health care reform efforts will bring incremental improvement, but reengineering prevention into health care will require deeper changes, including reconnecting medicine to public health services and integrating prevention into the management and delivery of care. Though change is painful, the successful transformation of medicine at the turn of the last century shows that it is possible. Ultimately, embedding prevention in the teaching, organization, and practice of medicine can stem the unabated, economically unsustainable burden of chronic disease.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

SOURCE INFORMATION

From the Stanford Prevention Research Center and the Department of Medicine, Stanford University Medical School, Stanford, CA.

The most contaminated surfaces in hotel rooms

An experiment of surfaces in hotel rooms finds television remotes to be among the most heavily contaminated with bacteria and items on housekeeping carts carry the potential to cross-contaminate rooms. Researchers from the University of Houston report the findings today at the 2012 General Meeting of the American Society for Microbiology.

“Hoteliers have an obligation to provide their guests with a safe and secure environment. Currently, housekeeping practices vary across brands and properties with little or no standardization industry wide. The current validation method for hotel room cleanliness is a visual assessment, which has been shown to be ineffective in measuring levels of sanitation,” says Katie Kirsch an undergraduate student at the University of Houston who presented the study.

As the public becomes increasingly concerned with public health, hotel room cleanliness and sanitation are becoming consideration factors for consumers when selecting a hotel room. Contact with contaminated surfaces is a possible mode of transmission of illness during outbreaks in hotels. This, combined with the lack of standardization of hotel room cleanliness, poses a risk for hotel guests, specifically immunocompromised individuals who are more susceptible to infection.

“Currently, housekeepers clean 14-16 rooms per 8-hour shift, spending approximately 30 minutes on each room. Identifying high-risk items within a hotel room would allow housekeeping managers to strategically design cleaning practices and allocate time to efficiently reduce the potential health risks posed by microbial contamination in hotel rooms,” says Kirsch.

The study was designed as the first step in applying the Hazard Analysis and Critical Control Points (HACCP) system to hotel room cleanliness. Originally developed by the National Aeronautics and Space Administration, HACCP is a systematic preventive approach that identifies potential physical, chemical and biological hazards and designs measurements to reduce these risks to safe levels.

Kirsch and her colleagues at the University of Houston, along with researchers from Purdue University and the University of South Carolina sampled a variety of surfaces from hotel rooms in Texas, Indiana and South Carolina. They tested the levels of total aerobic bacteria and coliform (fecal) bacterial contamination on each of the surfaces.

While some of the most contaminated samples, including the toilet and the bathroom sink, were to be expected, they also found high levels of bacterial contamination on the TV remote and the bedside lamp switch. Most concerning, some of highest levels of contamination were found in items from the housekeepers’ carts, including sponges and mops which pose a risk for cross-contamination of rooms. Surfaces with the lowest contamination included the headboard on the bed, curtain rods and the bathroom door handle. The researchers cannot say whether or not the bacteria detected can cause disease, however, the contamination levels are a reliable indicator of overall cleanliness.

Kirsch warns that this study is preliminary and is limited by the sample size, which included only 3 rooms in each state and 19 surfaces within each hotel room, but hopes that it is just the beginning of a body of research that could offer a scientific basis to hotel housekeeping.

“The information derived from this study could aid hotels in adopting a proactive approach for reducing potential hazards from contact with surfaces within hotel rooms and provide a basis for the development of more effective and efficient housekeeping practices,” says Kirsch.

 Katie Kirsch will participate in a live webcast media availability to discuss her research on Sunday, June 17, 2012 at 2:00 p.m. EDT. The webcast can be found online at www.microbeworld.org/asmlive.

Millions of women in the U.S suffer from on going painful UTI (urinary tract infections) every year. Now scientists think they may be caused by contaminated chickens.  

Try to eat organic chicken

So what’s the deal about “organic” versus “battery” or “free-range” chickens? It has to do with our poultry practices and food safety. The lowest on the ladder are battery chickens (the cheapest). These factory-farmed chickens are inhumanely raised in substandard living conditions and are force-fed or injected with growth hormones. Next up the rung are free-range chickens. As the names implies, these chickens have freedom to move about; but, they too are sometimes subjected to growth hormones. Organic chickens (the most expensive), the top rung, are humanely raised and fed natural foods and no the growth hormones.

Factory-farmed chickens are quite literally confined, unable to properly move about, eat, drink and defecate freely as they should. Disease becomes more common among battery chickens as a result of this confinement. This poultry practice in turn creates a greater need for antibiotics. Increased use of antibiotics eventually leads to bacteria mutating over time, becoming antibiotic resistant. When people are infected with the antibiotic strain, fewer medications are able to effectively treat the bacteria. We may shudder at the cost difference of a battery and an organic chicken, but the organic chicken is clearly the better option.

Last Thursday the Lancet published a multi-author meta analysis that is challenging the notion that increased HDL cholesterol levels offer protection against myocardial infarction (MI)(Voight 2012). Using genome-wide association studies from 100,000 individuals this group was able to find genes that functioned to increase serum HDL-cholesterol levels independently of other lipids associated with cardiovascular disease risk, such LDL-C and triglycerides. The group then ascertained whether or not the presence or absence of these genetic SNPs associated with HDL-C raising were also associated with protection from MI using SNP-to-biomarker and biomarker-to-MI relationships created from analyzing six prospective clinical studies. They found no association between gene variants exclusively related to HDL concentration and MI risk reduction risk of MI. However, they did find SNPs associated with LDL cholesterol were associated with reduced MI risk.

The devil is in the details 

This group analyzed data collected from their recent genome-wide association studies (GWAS) on more than 100,000 people finding14 SNPs with statistical evidence for influencing plasma HDL-C yet no association with triglycerides or LDL-C. Similarlyfor LDL-C, the team discovered 13 SNPs with statistical associations for influencing plasma LDL-C, independent of triglycerides or HDL-C. These identified SNPs were then evaluated individually for their weighted influence on changes in LDL-C or HDL-C per 1000,000 individuals. Using this data the group was able to create a ‘genetic score’ obtained from HDL/LDL-to-MI, SNP-to-biomarker, biomarker-to-MI relationships multiple prospective cohort trails.

Of the 14 HDL-C related SNPs tested, the endothelial lipase gene known as LIPG seemed to have the most direct impact on HDL concentrations. Carriers of the LIPG Asn396Se allele tended to have statistically significant increases in HDL-C VS non-carriers (0.14 mmol/L, p.oo5). Figure 1. represents the data collected from four different prospective cohort studies (FHS, CCHS, MDC, and ARIC) wherein blood concentration of HDL-C were assessed in carriers VS non-carriers of the LIPG Asn3996Ser allele which is known to increased HDL-C.

Just how much of an impact does the presence of this endothelial lipase SNP raise HDL cholesterol blood levels?

As you can readily see, carriers of the LIPG SNP do indeed have statistically significant increases in HDL-C VS non-carriers. However when HDL-C blood levels are reported as mg/dL, we can see that while there are statistical diferences in HDL-C, they respective increase is seemingly irrelevant from a clinical perspective. All other biomarkers being equal, should we really expect this small increase in HDL-C would translate into reduced incidence of MI? We know that HDL concentration is not as important as HDL “function”, and that increased HDL- concentration (i.e. blood levels mg/dL) are associated with, but not diagnostic of, HDL phenotype (Creider 2012).

At any rate, to adequately asses the correlation between risk of myocardial infarction and the presence of this HDL-C raising polymorophisms the team further analyzed data from six prospective cohort studies, involving 50,763 individuals. They calculated that carriers of this HDL-C raising allele would be expected to have a 13% reduction in risk of MI. However no such correlation was found. As such, the authors concluded that interventions designed to raise plasma HDL cholesterol- such as exercise- should not be assumed to reduce risk of myocardial infarction.

What can we make of this? 

For staters we know that HDL is much more than just a lipid garbage truck- functioning solely as a reverse cholesterol transporter. HDL is a anti-inflammatory and antioxidant lipoprotein. Should we ignore HDL’s protective and  pleiotropic nature because the presence of HDL raising SNPs are not correlated with reduced risk of an MI?  Does HDL-C really give us clues into HDL’s ‘function’-hence it’s cardioprotective capabilities? We’ve known for years that advanced lipoprotein particle testing offers added clinical insight into the function of these particles when compared to standard HDL-C plasma levels (Brunzell 2008).

We know that assessment of cholesteorl-to-protein ratio and HDL particle size are much more representative of HDL’s cardioprotective abilities versus plasma HDL-C (Scheffer 2011). For example individuals with metabolic syndrome and type 2 diabetes have reduced HDL particle size, cholesterol carrying and anti-inflammatory capacity;  exhibiting signs of “functionally impaired HDL.” Additionally new research suggests that HDL may function to improve blood sugar and insulin homeostasis- independent heart disease risk factors- through several different mechanisms (Drew 2012). HDL’s membrane bound lipoproteins ApoA-I and ApoA-II function to improve peripheral insulin sensitivity via a pancreatic beta cell dependent mechanism. Additionally HDL is known to enhance glucose uptake via an insulin-independent fashion, via binding to the muscle cell surface lipid- transporter ABCA1, increasing the activity of cellular energy sensor AMPK leading to enhanced mitochondria function and biogenesis.

In conclusion, it’s too early to definitively say that we should no longer aim to increase HDL-C levels in patients, particularly in patients with increased cardio-metabolic risk. We know that every single LDL particle render one atherogenic apolipoprotein B (ApoB), while HDL levels have varying concentrations of cardioprotective apoliproteins ApoA-I and ApoA-II (Drew 2012). Thus all LDL and VLDL particles have the potential to be atherogenic, while not all HDL particles are anti-atherogenic. HDL physiology- compared to LDL physiology- is arguably more pliotropic and complicated. Thus the presence of absence of a sinlge SNP pertaining to HDL physiology should not guide clinical treatment, especially when one understands that cardiovascular disease is the leading cause of mortality in industrialized nations.

References

(Creider 2012) Creider, J. C., Hegele, R. A., & Joy, T. R. (2012). Niacin: another look at an underutilized lipid-lowering medication. NATURE REVIEWS | ENDOCRINOLOGY, 1–12. doi:10.1038/nrendo.2012.22

(Brunzell 2008) Lipoprotein management in patients with cardiometabolic risk: consensus statement from the American Diabetes Association and the American College of Cardiology Foundation. (2008). Lipoprotein management in patients with cardiometabolic risk: consensus statement from the American Diabetes Association and the American College of Cardiology Foundation. (Vol. 31, pp. 811–822). doi:10.2337/dc08-9018

(Drew 2012) Drew, B. G., Rye, K.-A., Duffy, S. J., Barter, P., & Kingwell, B. A. (2012). The emerging role of HDL in glucose metabolism. NATURE REVIEWS | ENDOCRINOLOGY, 1–9. doi:10.1038/nrendo.2011.235

(Scheffer 2011) Scheffer, P. G., Tushuizen, M. E., Vermue, H. P. A., Schindhelm, R. K., Rustemeijer, C., & Diamant, M. (2011). Effect of three consecutive meals on the physicochemical properties of HDL and LDL in individuals with the metabolic syndrome and patients with type 2 diabetes, 1–8. doi:10.1038/ejcn.2011.114

(Voight 2012) Voight, B. F., Peloso, G. M., Orho-Melander, M., Frikke-Schmidt, R., Barbalic, M., Jensen, M. K., Hindy, G., et al. (2012). Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. The Lancet. doi:10.1016/S0140-6736(12)60312-2

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1lb of mixed berry and mango frozen

1 zest of lime

Juice of 1 fresh lime

1 can of coconut milk (organic)

1/4 cup of maple syrup (optional)

1 tablespoon vanilla

place all ingredients in a food processor or vita mix and process for three mints until creamy. transfer to glass dish and place in freezer for 15 mints before  serving.

Oxidative stress is the process when the cells are greatly damaged because of free radicals. We know that we can be affected by free radicals if the level of anti-oxidants is decreased in our system. It usually happens as we age, when we reached the age of thirty’s and above. The reason is because by the age of 26, the level of anti-oxidant level in our cells will be reduced by 10% every 10 years.

Oxidative Stress Symptoms

Oxidative stress is thought to contribute to the aging process, neurodegenerative diseases and certain cardiovascular diseases. These include:

• Tissue injury
• Cardiovascular Diseases such as hart attacks and strokes
• Hyperoxia
• Irradiation
• Neurodegenerative Diseases such as Alzheimer’s and Parkinson’s

Here are some diseases related to Oxidative Stress:

Prevent Oxidative Stress Symptoms

To prevent oxidative stress, you must have proper diet, exercise regularly and have the right supplement. By the time you reached the age of early thirty’s you must slow down from the usual life style you had.   If you can’t increase the level of anti-oxidants, you might as well stop the other factors that may affect your over all being. By boosting your immune system you can stop oxidative stress in your body by taking the right supplements.

 Foods High in Antioxidants

• All Vegetable
• All fruits
• Whole Grains
• Nuts
• Red Wine
• Red Capsicum
• Black and green Tea

Supplements that can reduce oxidative stress

• Vitamin A
  
• Vitamin C
• VitaminE
• Selenium
• Vitamin D3